Studies on the mechanism of Coxsackie B-3 virus-induced heart muscle disease will be performed in inbred Balb/c mice. Two strains of Coxsackie B-3 virus grow in the heart to equal titers although only one strain produces significant inflammation. The specific aims of this application are to determine the relative degree of cardiac injury produced by the myocarditic and nonmyocarditic strains of the virus and to correlate injury as measured by increased creatine kinase levels in the serum or by alterations in the electrocardiogram pattern with peak viral growth or mononuclear cell infiltration in the heart. If injury correlates with inflammation, I propose to (1) identify and isolate the immune lymphocytes causing maximum injury, (2) investigate the mechanism by which the myocarditic virus induces these immune lymphocytes but the nonmyocarditic virus does not, and (3) identify and isolate the antigens on myofibers recognized by the immune lymphocytes resulting in myofiber destruction. It is hoped that a thorough understanding of the properties of certain viruses which induce strong inflammatory responses may aid in diagnosis, prevention or treatment of viral myocarditis in humans.